Author + information
- James D. Fett, MD, MPH⁎ ()
- ↵⁎Hôpital Albert Schweitzer, Department of Adult Medicine, Deschapelles, Haiti, 2331 Mt. Hood Court Southeast, Lacey, Washington 98503
It is premature to attribute the recovery of 2 “postpartum cardiomyopathy” patients to the blocking effect of bromocriptine against prolactin and to assign causal relationship of 16 kDa prolactin to human peripartum cardiomyopathy (PPCM) (1,2).
Both patients in heart failure were treated with angiotensin-converting enzyme (ACE) inhibitor and beta-blocker drugs with apparent benefit possibly even before the use of bromocriptine. Most recent studies show that when PPCM is diagnosed in a timely fashion and treatment is instituted with diuretic, ACE-inhibitor, and beta-blocker drugs almost everyone improves, almost everyone survives, and over 50% completely recover left ventricular systolic function (3,4). Furthermore, the rate of recovery in many conventionally treated PPCM patients is often very comparable to that seen in the 2 cases reported, without bromocriptine in the picture.
I urge attention to the issue of the role of prolactin-suppression with bromocriptine in the development of PPCM through carefully controlled, randomly assigned, double-blinded placebo studies, after addressing the following issues:
1) Is it safe to use bromocriptine in the early postpartum period? A number of reports indicate acute myocardial infarction has complicated the use of bromocriptine in healthy mothers for lactate suppression (5). What will be the short-term and long-term effects of circumventing the important natural effects of prolactin on the involution process of the post-gravida uterus?
2) Are the reputedly abnormal 16-kDa and the naturally occurring 23-kDa derivatives of prolactin metabolism harmful? Have sufficient studies been accomplished to be reasonably confident that is the case?
3) Is serum prolactin significantly elevated in PPCM patients either antepartum or post-partum as compared with healthy non-PPCM patients? If so, as might be the case because of efforts to stimulate lactation in an acutely or subacutely ill mother, does that elevation constitute a causal relationship to PPCM rather than a non-causal physiological response?
It is also important to pursue these issues, because if third world mothers with PPCM—where the incidence is higher—were to inhibit lactation through the use of bromocriptine or simply cease breastfeeding in an effort to eventually decrease prolactin, many of their newborns would die of malnutrition as a consequence of the inability to provide a substitute for breast milk (6).
Please note: Charitable contributions and volunteer services were received from Hôpital Albert Schweitzer, Pittsburgh, Pennsylvania.
- American College of Cardiology Foundation